These patients often suffer from left heart failure, intracranial hemorrhage, infective endocarditis, aortic dissection and rupture, and coronary artery and cerebrovascular disease. The natural history has been described in coarctation patients before correction became imperative. As BAV and CoA are two related abnormalities with both origins in the neural crest cells, they seem to be part of a broader aortopathy. Apoptosis of smooth muscle cells might contribute to weakness of the wall which might explain the high cardiovascular morbidity in BAV patients. BAV patients have structural changes of the aortic media such as thinner elastic lamellae and greater distance between the lamellae. In BAV too aortic wall changes seem to take place at least partly independent from hemodynamics. More research has been conducted on the aortic vessel wall in BAV, which often coincides with CoA as discussed below. The underlying cause of these histological abnormalities is most probably so-called cystic media necrosis. ![]() There is evidence to support an inherent vessel wall weakness that occurs separately from hemodynamical changes. Small studies have compared pre- and post-stenotic tissue to assess the histological abnormalities and tried to account for the influence of blood pressure. Comparatively little attention has been directed to the prevalence, range, or degree of histological changes in the aortic wall (arterial media) of patients with CoA.
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